Studies into the mechanisms involved in the development and maintenance of hypertension are being conducted in the New Zealand genetically hypertensive strain of rat. Observations to date indicate that differences in intrarenal prostaglandin metabolism are not responsible for either the hypertensive state or for the renal vascular hypersensitivity to exogenous prostaglandins. For reasons as yet unknown, renal blood flow is lower in adult NZ GH rats in normotensive controls; however, in 25-day old rats, renal blood flow and vascular resistance of the hypertensive and normotensive strains do not differ. Bilateral renal denervation delays the development of hypertension but does not prevent it or alter the final blood pressure level; urinary output of prostaglandin E2 and kallikrein is not altered by the renal denervation.